Elite athletes harbor performance-enhancing gut microbe that turns lactate into fat

Updated: Nov 15, 2019

Publishing venue: Nature Medicine 2019; 25(7): 1104-1109

Link: https://www.nature.com/articles/s41591-019-0485-4

Author(s) and Title: Scheiman J., et al. Meta-omics analysis of elite athletes identifies a performance-enhancing microbe that functions via lactate metabolism.

How It’s Depleted: Passing high deuterium glycogenic lactic acid from circulation to atypical Veillonella bacteria of the gut that ferment it to propionate, while discriminating against and retaining deuterium by ATPase nanomotors [1] for their growth [2]. Deuterium depletion occurs by returning low deuterium ketogenic propionic acid to the circulation for terminal oxidation into deuterium depleted metabolic water and CO2 in the mitochondria/peroxisomes of host cells.

Deutenomics: During exercise lactate (lactic acid; CAS Number: 50-21-5; Chemical formula: C3H6O3; Molar mass: 90.078 g; CH3-CH(OH)-CO2H) gets expelled from the arterial circulation in the splanchnic area to be consumed rapidly by gut bacteria. As a result there is less build-up of lactate in the arterial circulation of professional athletes during exercise who train partially by propagating lactate fermenting bacteria in the gut. Lactate is fermented into low deuterium propionate (propionic acid; CAS Number: 79-09-4; Chemical formula: C3H6O2; Molar mass: 74.079 g; CH3-CH2-CO2H) by fermentation in atypical Veillonella [3]. Membrane transport and reversible rapid conversions of lactate and pyruvate occur via the low control coefficient [4] monocarboxylate transporters and lactate dehydrogenase along concentration gradients. Lactate efflux is significant through multiple membranes whereby the little rise in lactate levels in the circulation of athletes is the result of robust bacterial lactate fermentation into low deuterium propionate via acetyl-CoA production [5]. Lactate is intensely produced in runners but it isn’t getting built up after atypical Veillonella propagation and adaptation by the human gut that provides a high turnover for deuterium. Apnea and thus whole body anaerobic lactate production is also part of the above deuterium depleting biochemical substrate-product architecture and transport during sleep and seizures in the brain. The above biochemical mechanisms are interpreted as bypass pathways of the deuterium-sparing Cori cycle, which is the recycling of lactic acid to high deuterium containing glucose in the mammalian liver.


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Keywords: Lactate-propionate cycling; Cori cycle; Metabolic ketosis; System’s Biology of Deuterium depletion; Autonomic biological processing of deuterium; Deutenomics; Deutenomic data interpretation; Brain metabolism; Sleep; Petit mal seizure;

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